Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Genotypic and Phenotypic Diversity as a Function of CRISPR-Directed Gene Knock-Out of NRF2 in Pancreatic Adenocarcinoma Cells, a Feasibility Study.

Biomolecules - 3 Jun 2026

McGill London P, Banas Kelly H, Tiesi Gregory, Kmiec Eric B

Abstract excerpt

Pancreatic ductal adenocarcinoma (PDAC) presents unique treatment challenges, often due to the development of anti-cancer drug resistance. Previously, we demonstrated that CRISPR-directed gene ablation disabled the master regulator gene NRF2, a transcription factor known to control drug resistance in squamous cell carcinoma tumor cells, and restored chemosensitivity. In this short study, we evaluated a broad...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Carcinoma, Pancreatic Ductal
Share to CRISPR-Cas Systems

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Deoxycytidine

Share to Feasibility Studies

Share to Gemcitabine

Share to Gene Knockout Techniques

Share to NF-E2-Related Factor 2

Share to RNA, Guide, CRISPR-Cas Systems

Source

Open in PubMed Open full text

Identifiers

PMID: 42352295
DOI: 10.3390/biom16060828
PMCID: PMC13297238

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Genotypic and Phenotypic Diversity as a Function of CRISPR-Directed Gene Knock-Out of NRF2 in Pancreatic Adenocarcinoma Cells, a Feasibility Study.PMID 42352295Read ↗

Targeted CRISPR screening identifies PRMT5 as synthetic lethality combinatorial target with gemcitabine in pancreatic cancer cellsSemantic proximity Read ↗

Targeted CRISPR screening identifies PRMT5 as synthetic lethality combinatorial target with gemcitabine in pancreatic cancer cellsSemantic proximity Read ↗

Characterization and therapeutic suppression of KEAP1-NRF2-driven resistance to KRAS inhibitors in pancreatic and lung cancerSemantic proximity Read ↗

Inhibiting NR5A2 targets stemness in pancreatic cancer by disrupting SOX2/MYC signaling and restoring chemosensitivitySemantic proximity Read ↗

CRISPR-Cas9 for selective targeting of somatic mutations in pancreatic cancersSemantic proximity Read ↗

Efficacy of CRISPR-Cas9 Gene Editing for Targeting KRAS Mutations in Pancreatic Cancer: A systematic reviewSemantic proximity Read ↗

Pharmacologically targeting KRAS <sup>G12D</sup> in PDAC models: tumor cell intrinsic and extrinsic impactSemantic proximity Read ↗

Targeting APE1 endonuclease activity impairs metastasis and enhances genotoxic therapy response in pancreatic cancerSemantic proximity Read ↗

Brucein D augments the chemosensitivity of gemcitabine in pancreatic cancer via inhibiting the Nrf2 pathwaySemantic proximity Read ↗

Nrf2 is overexpressed in pancreatic cancer: implications for cell proliferation and therapy.Semantic proximity Read ↗

CRISPR-Cas9 Screen Identifies DYRK1A as a Target for Radiotherapy Sensitization in Pancreatic CancerSemantic proximity Read ↗

Tumor cell-intrinsic stress states drive sensitivity to CAR T cell-therapy in pancreatic cancerSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.